Fig. 4. Expression of comm-HP in either neurones or midline cells leads to guidance defects at the midline. (A) Sema2b neurones in the wild-type stage 16 embryo. (B) When comm-HP is driven in midline cells, the Sema2b neurones make crossing errors. The commissures are thinner and occasionally fail to form, as do sections of the longitudinal tract. Growth cone stalling at the midline is also seen (arrow). (C) When comm-HP is driven in neurones, the commissures are more severely affected and longitudinal sections can be completely absent. (D,E) Expression of comm-HP in neurones in a comm heterozygous background results in an enhanced phenotype where crossing errors are frequent and stalling occurs (arrow). Commissures and longitudinal sections are often absent or significantly reduced. (F-J) BP102 staining of the ventral nerve cord at (F-H) stage 13 or (I,J) stage 16. Arrows indicate thinner commissures, arrowheads indicate axon stalling. (F) Wild-type embryo. (G) When comm-HP is expressed in neurones, some axon stalling around the commissures is evident (arrowhead) together with thinner longitudinals and occasional thinner commissures (arrow). (H) This phenotype is enhanced when comm-HP is expressed in neurones in a comm heterozygous background. At later stages in development, some axon stalling and thinner longitudinals are observed when comm-HP is expressed in (I) neurones or (J) midline cells. All panels show a dorsal view of the CNS and are oriented with anterior upwards.